Recently many studies have reported that Indole ethyl isothiocyanates (Singh et al, British journal of cancer, 2008, 99:1823-1831; Gynecologic Oncology, 2008, 109:240-249; Bioorg and Med Chem Lett 2007, 17:5846-5852) inhibited the growth of ovarian, neuroblastoma, prostate, pancreatic, and breast cancer cells in culture by inducing apoptosis. Phenyl ethyl isothiocyanate (PEITC) has been shown to induce apoptotic cell death in HeLa cells in a time- and concentration-dependent manner, through rapid and transient induction of caspase-3-like activity and activation of JNKs. The involvement of caspases, including caspase-3 and caspase-8, and JNKs in phenyl ethyl isothiocyanate (PEITC) induced apoptosis has also been established in other cell lines including human leukemia HL-60 cells. PEITC induces apoptosis potently in a p53-deficient PC-3 human prostate cancer cell line mediated by ERKs.
The anti-carcinogenic potential of isothiocyanates (ITCs) are demonstrated further by the finding that their metabolites formed in vivo possess similar, if not more potent, anticarcinogenic activity in cultured cells or animal models. ITCs are rapidly metabolized mainly through the mercapturic acid pathway in both humans and animals, giving rise to various dithiocarbamate metabolites, such as cysteinyl glycine, cysteine, and N-acetylcysteine conjugates which are excreted in the urine.